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The Bradyarrhythmias: Disorders of the Atrioventricular Node

Chapter 252 | Part 6: Disorders of the Cardiovascular System · Part 6 – Cardiovascular Disorders · Chapter 252

Key Clinical Points

  1. The AV node acts as an electrical 'gatekeeper' using specialized cells and gap junctions (connexin-40) to create a necessary delay between atrial and ventricular activation.
  2. First-degree AV block is defined by a PR interval >200 ms with all atrial impulses conducted to the ventricle.
  3. Mobitz I (Wenckebach) shows progressive PR prolongation until a dropped beat; Mobitz II features a fixed PR interval before a drop and is typically infranodal (associated with QRS widening).
  4. Inferior MI typically causes intranodal block (narrow escape, >40 bpm), while anterior MI leads to infranodal block (wide escape) with higher mortality.
  5. Vagal tone during sleep can cause transient AV block; atropine improves conduction in the AV node but may impair infranodal conduction.
  6. Permanent pacing is indicated for symptomatic bradycardia, irreversible second- or third-degree AV block, and asymptomatic bifascicular block with intermittent third-degree block.
  7. Leadless pacemakers are suitable for single-chamber ventricular pacing to preserve AV synchrony in patients with AV block but without sinus node dysfunction.
  8. Electrophysiologic study (His bundle electrogram) distinguishes intranodal (AH prolongation) from infranodal (HV prolongation) block.
  9. Lyme carditis typically presents with AV block that improves within 1 week of antibiotic therapy.
  10. Endocarditis-associated block requires urgent surgical consultation to rule out perivalvular abscess.

DEFINITION & OVERVIEW

• Definition (Harrison's 22e): The AV node is specialized for slow conduction of the action potential to create a delay between atrial and ventricular activation. • Anatomy: ◦ Size: Small region (~1 imes 3 imes 5 mm) located beneath the right atrial endocardium at the apex of the triangle of Koch. ◦ Triangle of Koch Landmarks: Coronary sinus ostium (posterior), septal tricuspid valve annulus (anterior), and tendon of Todaro (superior). ◦ Subdivisions: Lower nodal bundle and compact node. ◦ Extensions: Rightward inferior extension toward coronary sinus; leftward extension along the tendon of Todaro. • Conduction Pathway: ◦ Compact AV node → penetrating AV bundle (traverses central fibrous body) → His bundle (along ventricular septum). ◦ His bundle → Right Bundle Branch (RBB) → moderator band. ◦ His bundle → Left Bundle Branch (LBB) → broad subendocardial sheet on septal LV. • Cellular Electrophysiology: ◦ Resting membrane potential: ~–60 mV. ◦ Action Potential: Low amplitude, slow phase 0 upstroke, spontaneous phase 4 diastolic depolarization. ◦ Ion Channels: Lack robust I_{K1} and fast Na^{+} current; Phase 0 driven by L-type calcium (I_{Ca-L}). ◦ Coupling: Tenuous due to sparse gap junction channels (predominantly connexin-40). • Table 252-1: Electrocardiographic Classification of Atrioventricular (AV) Block ◦ First-Degree: All atrial impulses conducted; PR interval >200 ms; delay usually in AV node. ◦ Second-Degree Type I (Mobitz I/Wenckebach): Progressive PR prolongation until drop; associated with QRS widening; delay in AV node. ◦ Second-Degree Type II (Mobitz II): Fixed PR interval before drop; associated with QRS widening; infranodal. ◦ Third-Degree: Complete interruption of conduction between atria and ventricles (complete heart block).

EPIDEMIOLOGY

• Age-Related Changes: ◦ Senile degeneration (idiopathic fibrosis/calcification) is the most common cause in elderly patients. ◦ Progression typically begins in 4th decade; accelerated by atherosclerosis, hypertension, and diabetes mellitus. • Congenital & Genetic: ◦ Associated with complex congenital heart defects (e.g., TGA, ASD, VSD). ◦ Linked to heritable neuromuscular diseases (myotonic dystrophy, Kearns-Sayre syndrome). ◦ Genetic markers: Mutations in SCN5A and other loci on chromosomes 1 and 19. • Acquired: ◦ Rare in healthy adults (1 per 5000/year) but common in patients with myocardial ischemia, infiltrative disease, or autoimmune conditions.

ETIOLOGY & PATHOPHYSIOLOGY

• Fibrosis & Calcification: ◦ Lev's disease: Proximal bundle branch fibrosis. ◦ Lenègre's disease: Sclerodegenerative process in distal portions of bundle branches. ◦ Calcification: Aortic valve annulus (common); mitral valve (less common). • Iatrogenic Causes: ◦ Surgery: Highest risk in aortic and tricuspid valve surgery. ◦ Procedures: TAVR, alcohol septal ablation, and catheter ablation for atrial arrhythmias (risk <1%). ◦ Medications: Beta-blockers, verapamil, diltiazem, digoxin. • Ischemic Causes: ◦ Inferior MI → AV node block → Narrow escape (>40 bpm) → Usually reversible with meds. ◦ Anterior MI → Infranodal/Bundle branch block → Wide complex, unstable rhythm → High mortality; temporary pacing indicated. • Infectious & Infiltrative: ◦ Lyme carditis (Borrelia burgdorferi): Typically improves within 1 week of antibiotics. ◦ Endocarditis: Requires urgent surgical consultation if perivalvular abscess is suspected. ◦ Others: Viral myocarditis, Chagas' disease, Toxoplasmosis. ◦ Infiltrative: Sarcoid, Amyloid, Hemochromatosis. • Autoimmune & Neuromuscular: ◦ SLE, Rheumatoid arthritis, Systemic sclerosis. ◦ Myotonic dystrophy, Kearns-Sayre syndrome, Erb's dystrophy. • Table 252-2: Causes of AV Block ◦ Fibrosis/Sclerosis: Senile degeneration (Lev's), Lenègre's, Calcification. ◦ Iatrogenic: Surgery, TAVR, Ablation, Medications (Beta-blockers, Digoxin). ◦ Infectious: Lyme carditis, Endocarditis, Myocarditis, Chagas' disease. ◦ Infiltrative/Inflammatory: Sarcoid, Amyloid, Rheumatologic diseases, Neuromuscular diseases.

CLINICAL FEATURES

• Symptomatic Presentation: ◦ Fatigue, Syncope, Death from asystole. ◦ Worsening heart failure, Angina, Intolerance to essential medication. • Asymptomatic Presentation & Pacing Criteria: ◦ Acquired CHB with cardiac enlargement or LV dysfunction. ◦ Waking heart rates ≤40 beats/min (specifically for AV node level). ◦ Asymptomatic 2nd-degree block if infranodal or associated with wide QRS. ◦ Profound 1st-degree AV block with LV dysfunction where shorter interval improves hemodynamics. ◦ Neuromuscular diseases (myotonic dystrophy, Kearns-Sayre) with conduction system predilection.

DIFFERENTIAL DIAGNOSIS

• Sinus Node Dysfunction (SND) vs. AV Block: ◦ Single-chamber pacemakers may be used for pure SND in low-risk patients. ◦ Note: Fibrosis of the sinus node is often associated with fibrosis of the AV node; many SND patients will eventually develop AV block.

DIAGNOSTIC APPROACH

  1. Initial Assessment: Determine if patient is symptomatic.
  2. Symptomatic Path: → Symptom? Yes → Proceed to AV block treatment algorithm.
  3. Asymptomatic Path (Evaluation): → Symptom? No → Exercise testing (Class IIa). → If Intranodal identified → Proceed to AV block treatment algorithm. → If Infranodal identified → Electrophysiology study (Class IIb).
  4. Asymptomatic Path (Refinement): → If EP Study shows Infranodal → Proceed to AV block treatment algorithm. → If EP Study shows AV node → Observe.
  5. Specialized Testing: → Use Hist Bundle Electrogram to distinguish Intranodal (AH prolongation) from Infranodal (HV prolongation) block.

MANAGEMENT & TREATMENT

  1. Acute Management: → Symptomatic patients → Immediate intervention. → Lyme carditis → Antibiotics (improvement typically within 1 week). → Endocarditis with suspected abscess → Urgent surgical consultation. → Anterior MI with high-grade block → Temporary pacing indicated.
  2. Permanent Pacing Indications: → Symptomatic bradycardia. → Irreversible second- or third-degree AV block. → Asymptomatic bifascicular block with intermittent third-degree block.
  3. Pacing Strategy (Decision Tree): → Marked first-degree AV block: → Symptom? Yes → Permanent pacing (Class I). → Symptom? No → Lamin A/C or neuromuscular disease? Yes → Permanent pacing (Class IIb). → Symptom? No → Lamin A/C only? Yes → Permanent pacing (Class III). → Symptom? No → None of above → Observation. → Mobitz I & II block: → Symptom? Yes → Permanent pacing (Class IIb). → Symptom? No → Neuromuscular disease? Yes → Permanent pacing (Class IIb). → Symptom? No → No neuromuscular → Observation. → Complete heart block / Infranodal block: → Symptom? Yes → Permanent pacing (Class I). → Symptom? No → Neuromuscular disease? Yes → Permanent pacing (Class IIb). → Symptom? No → No neuromuscular → Observation.
  4. Advanced Pacing Techniques: → Left bundle branch area pacing: Target specialized conduction system to achieve narrow QRS complex.

PROGNOSIS & COMPLICATIONS

• Infarction Prognosis: → Inferior MI (AV node) → Better prognosis, usually reversible. → Anterior MI (Infranodal) → Higher mortality, often requires pacing. • Pacemaker Complications: → Lead fracture, infection, and failure of the device.

SPECIAL POPULATIONS

• Neuromuscular Diseases: → Myotonic dystrophy, Kearns-Sayre syndrome, Erb's dystrophy. → These patients may require pacing even if asymptomatic due to progressive conduction tissue disorder.

KEY PEARLS & CLINICAL TRAPS

• Anatomical Rule: Inferior MI → AV node (narrow escape); Anterior MI → Infranodal (wide escape). → Vagal Influence: High vagal tone during sleep can cause transient AV block; use of atropine may improve conduction in the AV node but potentially impair infranodal conduction. → Leadless Technology: Useful for single-chamber ventricular pacing to preserve AV synchrony in patients without sinus node dysfunction.\ → Clinical Rule: Symptomatic high-grade block or infranodal block are primary drivers for permanent pacing.

Reference Tables

TABLE 252-1 Electrocardiographic Classification of Atrioventricular (AV) Block First-Degree AV Block All atrial…

Harrison's 22e, p.1925

  • First-Degree AV Block
  • All atrial impulses are conducted to the ventricle
    PR interval is abnormally long (>200 ms)
    AV delay usually occurs within the AV node
  • Second-Degree AV Block (intermittent failure of conduction between
    atrium and ventricle)
  • Two subtypes
    Type I/Mobitz I/Wenckebach block: progressive prolongation of the PR interval
    until loss of conduction occurs
    Type II/Mobitz II: fixed PR interval precedes loss of conduction
    Usually associated with QRS widening
  • Third-Degree AV Block (complete heart block)
  • Complete interruption of conduction between atria and ventricles